Immunity from exposure to similar virus strains?

[Swamp Thing]

TL;DR

Is it possible that people who have been exposed to less virulent strains of virus that are similar to, eg, Covid-19, may be more immune to it than those who haven't been exposed?
If so, can we define a concept like "immunosimilarity" to quantify this effect?

The summary says it all. But to give an example, imagine a mild virus that has gone the rounds of Region A. Later it makes its way to Region B, and immediately mutates into a more rapidly spreading strain that puts B's inhabitants at great risk. Now that new strain travels back to Region A. Question is, could it be that the new strain would find it harder to get a foothold in Region A, simply because its milder ancestors have triggered people's immune systems there already?

 

[jedishrfu]

We don't know that. While it may appear that our bodies get immunity from viral or bacterial illness we just had if we survive that is. We may then have some immunity to a mutated version in the future depending on how mutated it was.

This is the reason they call it the novel Coronavirus as we've not encountered a virus of this kind before and so we have little protection against it. Doctors have said it resembles SARS but yet is different enough from SARS to get its own name of SARS-cov2.

https://en.wikipedia.org/wiki/Severe_acute_respiratory_syndrome_coronavirus_2

Our immune systems target specific receptors on the virus and during mutations some will have changed but others remain and so our immune system will recognize the invader but may not be able to completely latch on until our immune system adapts.

https://en.wikipedia.org/wiki/Viral_entry

https://kidshealth.org/en/parents/immune.html

 

[Rive]

If so, can we define a concept like "immunosimilarity" to quantify this effect?

As some kind of very limited 'cross-immunity' was observed between closely related strains of flu.
It was more about a less severe illness than immunity, though. So it would be better to call it 'cross protection' instead.

The small changes that occur from antigenic drift usually produce viruses that are closely related to one another, which can be illustrated by their location close together on a phylogenetic tree. Influenza viruses that are closely related to each other usually have similar antigenic properties. This means that antibodies your immune system creates against one influenza virus will likely recognize and respond to antigenically similar influenza viruses (this is called “cross-protection”).

 

[Ygggdrasil]

Summary:: Is it possible that people who have been exposed to less virulent strains of virus that are similar to, eg, Covid-19, may be more immune to it than those who haven't been exposed?
If so, can we define a concept like "immunosimilarity" to quantify this effect?

The summary says it all. But to give an example, imagine a mild virus that has gone the rounds of Region A. Later it makes its way to Region B, and immediately mutates into a more rapidly spreading strain that puts B's inhabitants at great risk. Now that new strain travels back to Region A. Question is, could it be that the new strain would find it harder to get a foothold in Region A, simply because its milder ancestors have triggered people's immune systems there already?

The general answer is yes. For example, this is what happens with seasonal influenza virus. It goes though the Northern hemisphere, migrates to the Southern Hemisphere during the summer months for the Northern hemisphere, and by the time it returns for the Northern Hemisphere's winter the following year, it has acquired mutations that allow it to evade immunity from the previous year.

For COVID-19 specifically, we know that exposure to other similar viruses do not confer immunity. In studies with monkeys, infection with COVID-19 provides immunity to the disease in the short term, though studies on similar viruses suggest that the immunity can wane over the course of a few years.

Prior exposure to a similar virus can sometimes provide a partial protective effect and make subsequent infection more mild. However there is also the case where exposure to a similar virus can exacerbate infections from other strains of the virus (a phenomena known as antibody dependent enhancement, which is seen for the various strains of Dengue virus). One reason why it is so important to test new vaccines is to determine whether they are actually protective or whether they might cause antibody dependent enhancement.

 

[phyzguy]

The answer to your question is clearly yes in some cases. This is how vaccines were first used - it was discovered that people who had been infected with cowpox were immune to smallpox, prompting Edward Jenner to intentionally infect people with cowpox so they would be immune to smallpox. That's why we call them vaccines, from the Latin word vacca for cow. As usual, the devil is in the details. It depends how similar the two viruses are.

 

[Laroxe]

We don't really develop immunity to a virus, we develop a range of antibodies to different parts of the virus and these antibodies have different levels of effectiveness in preventing illness. The antibodies we produce tend to be highly specific to the virus that caused their production, and some virus variants may escape the action of some of the antibodies.

The antibodies do seem to decay quite rapidly but we should also have developed a range of "immune memory" cells which significantly shorten the time needed to produce a good antibody response. So people may still become infected, but will tend to clear the virus before they become seriously ill. Some of the memory cells work at the level of recognition of the virus, these cells recognise the virus whatever its variant, then the way in which our immune system works, the presence of the virus let's the immune cells refine the antibodies.
We know that with Covid some antibodies produced to other Coronaviruses can bind to the Covid-19 virus but none appear to do so at a level that provides significant protection, in fact some of the antibodies produced to the actual Covid-19 virus don't seem to do much. We produce antibodies that bind to the virus capsule but they don't appear to do much, that's why the spike protein was used in vaccines.